Volume 24, Issue 5

Cholinergic signaling mediated by nicotinic receptors has been associated to a large number of physiological and behavioral processes such as learning, memory, attention, food-intake and mood disorders. Although it is well established that many nicotinic actions are mediated through an increase in serotonin (5-HT) release, the physiological mechanisms by which nicotine produces these effects are still unclear. The dorsal raphe nucleus (DRN) contains the major amount of 5-HT neurons projecting to different parts of the brain. DRN also contains nicotinic acetylcholine receptors (nAChRs) located at somatic and presynaptic elements. Nicotine produces both inhibitory and excitatory effects on different subpopulations of 5-HT DRN neurons. In this review, we describe the presynaptic and postsynaptic mechanisms by which nicotine increases the excitability of DRN neurons as well as the subtypes of nAChRs involved. We also describe the inhibitory effects of nicotine and the role of 5-HT 1A receptors in this effect. These nicotinic actions modulate the activity of different neuronal subpopulations in the DRN, changing the 5-HT tone in the brain areas where these groups of neurons project. Some of the physiological implications of nicotine-induced 5-HT release are discussed.

Over the past decade, the function of the cytoskeleton has been studied extensively in developing and mature neurons. Actin, a major cytoskeletal protein, is indispensable for the structural integrity and plasticity of neurons and their synapses. Disruption of actin dynamics has significant consequence for neurons, neuronal circuits, and the functions they govern. In particular, cell adhesion molecules, members of the Rho family of GTPases, and actin-binding proteins are important modulators of actin dynamics and neuronal as well as behavioral plasticity. In this review, we discuss recent advances in Drosophila that highlight the importance of actin regulatory proteins in mediating fly behaviors such as circadian rhythm, courtship behavior, learning and memory, and the development of drug addiction.

The Golgi apparatus (GA) is a pivotal organelle in cell metabolism, functioning not only in the processing and transportation of cargoes but also in ion homeostasis, cell apoptosis, and stress sensing. We are interested in the intricate role of GA and the recently present novel concept of ‘GA stress’. GA shows various morphological alterations in many neurodegenerative diseases and cell apoptosis induced by biochemical reagents, mechanisms in which oxidative stress is strongly involved. In turn, the structural changes and morphological alterations of the GA could also transduce stress signals. Therefore, besides the biochemical changes, more attention should be paid to the morphological alterations of the GA itself during pathological processes and diseases. The Golgi reassembly and stacking proteins (GRASPs) have been identified as important components acting in the transformation of Golgi structure, and they may thus affect the Golgi functions and cell behavior. In this review, we will discuss the intricate role of the GRASPs in remodeling the GA morphology and focus on their mechanisms and effects in the processes of Golgi stacking, mitosis, cell apoptosis, and cargo secretion. We would also like to provide a further prospective of their potential biological values in neurodegenerative diseases.

In the brain, the four subunits of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor, glutamate A 1 (GluA 1 ), GluA 2 , GluA 3 , and GluA 4 form functionally different tetramers. Of these, GluA 1 is very important. It forms calcium-permeable (without GluA 2 ) AMPA receptors and induces the trafficking and integration of AMPA receptors within synaptic membranes. Increased GluA 1 expression and their phosphorylation are common mechanisms for the treatment of Alzheimer’s disease, schizophrenia, depression, and chronic drug addiction. Moreover, GluA 1 is also involved in pain and epilepsy. Increased phosphorylation of serine 831 in the GluA 1 receptor is a mechanism necessary to alleviate Alzheimer’s disease and depression. GluA 1 -/- knockout mice are used as a model of schizophrenia. A decrease in the total cell AMPA receptor currents and phosphorylation of serine 845 of GluA 1 is observed in chronic drug addiction. Increased expression of GluA 1 causes pain and is involved in epilepsy. GluA 1 -promoting AMPA receptor potentiators could be used to treat Alzheimer’s disease and memory loss. In conclusion, GluA 1 agonists or antagonists might be effective in various disorders and conditions of the central nervous system that are based on GluA 1 status at the synaptic region.

It has been almost 40 years since Barker, Jalinous, and Freeston designed and used the first device of transcranial magnetic stimulation (TMS). From then until now, this technique has evolved vertiginously, appearing a lot of new protocols and device modifications, which associated with new technologies complement and enhance the versatility of this technique. TMS has demonstrated to be a safe technology and become a key tool in the study of the complex brain processes. Despite this, it is as a therapeutic tool where this technique has caused a revolution. In this regard, this type of non-invasive brain stimulation has been proven useful in a variety of neurodegenerative and psychiatric disorders due to its biochemical, molecular, and cellular effects, with depression being the paradigm of the therapeutic effectiveness of this technique. This review focuses on a detailed vision of how this type of radiation modifies different biochemical and cellular processes that induce the mechanisms and pathways underlying the therapeutic effects of TMS.

With increasing use of various techniques to record optically and electrophysiologically from awake behaving animals and the growing developments of brain-machine interfaces, one might wonder if the use of acute-slice physiology is on its deathbed. Have we actually arrived at a stage where we can abandon the use of acute slices, with most of the information about brain functions coming from in vivo experiments? We do not believe that this is the case, given that our understanding of the nuts and bolts of the nervous system, such as ion channels and transporters in near-native state, neuronal compartmentalization, and single-neuron computation, is far from complete. We believe that in the foreseeable future, questions in these fields will still be best addressed by acute-slice physiology. We approach this review from the perspective of improving acute-slice physiology so it can continue to provide relevant and valuable contributions to neuroscience. We conclude that the death of acute-slice physiology is an obituary prematurely written, merely due to waxing and waning trends in science and the shortsightedness of investigators. Acute-slice physiology has at least one more life to live after the hype around new techniques has passed, but it needs to reinvent itself in light of current knowledge.

Here, we present a state-of-the-art review of the research performed on the brain-computer interface (BCI) technologies with a focus on signal processing approaches. BCI can be divided into three main components: signal acquisition, signal processing, and effector device. The signal acquisition component is generally divided into two categories: noninvasive and invasive. For noninvasive, this review focuses on electroencephalogram. For the invasive, the review includes electrocorticography, local field potentials, multiple-unit activity, and single-unit action potentials. Signal processing techniques reviewed are divided into time-frequency methods such as Fourier transform, autoregressive models, wavelets, and Kalman filter and spatiotemporal techniques such as Laplacian filter and common spatial patterns. Additionally, various signal feature classification algorithms are discussed such as linear discriminant analysis, support vector machines, artificial neural networks, and Bayesian classifiers. The article ends with a discussion of challenges facing BCI and concluding remarks on the future of the technology.

Minocycline is a semisynthetic second-generation tetracycline derivative, and many publications provide evidence of its successful neuroprotection in a variety of animal models. We searched PubMed and Chinese CNKI databases from January 1992 to May 2012 for studies on minocycline in neurodegenerative diseases in rodents. A meta-analysis that adopted weighted Cohen’s d effect sizes, percent overlap, Fail-Safe N statistics, and confidence intervals was conducted. In total, 16 English and 3 Chinese articles with high or medium quality were included in this meta-analysis. The treatment benefits for rodents from low-dose (5 mg/kg/day), moderate-dose (45, 50, or 55 mg/kg/day), and high-dose (90 mg/kg/day) minocycline were larger in Huntington’s disease, Alzheimer’s disease, and stroke mouse models, respectively. In rats, a moderate dose (45 mg/kg/day) of minocycline was most effective. In conclusion, minocycline exerts neuroprotective effects in rodent models of neurodegenerative diseases. Anti-inflammatory, antiapoptotic, and antioxidant activities are discussed as the basis of this effect. However, there is insufficient information from these animal models on side effects of minocycline therapy.